Can increased intestinal permeability and low-grade endotoxemia be the triggering pathogenesis in isolated coronary artery ectasia
Yükleniyor...
Dosyalar
Tarih
2023
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Lippincott Williams & Wilkins
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Purpose
Isolated coronary artery ectasia (ICAE) is a rare coronary artery disease (CAD) encountered during coronary angiography. Although many mechanisms have been suggested today that may be associated with ICAE, the underlying pathogenesis has not been fully understood. In this study, we aimed to reveal the possible relationship between intestinal permeability and ICAE.
Methods
Of the 12 850 patients who underwent coronary angiography, 138 consecutive patients with ICAE and 140 age- and sex-matched subjects with normal coronary arteries as the control group and 140 subjects with stenotic CAD were included in the study.
Results
Serum zonulin and lipopolysaccharide levels were significantly higher in patients with ICAE than in the control group and CAD group. Additionally, zonulin and lipopolysaccharide levels were significantly higher in the CAD group than in the ICAE group. In the correlation analysis, serum zonulin levels were correlated with the mean diameter and length of the ecstatic segment. In multivariate analysis, zonulin and lipopolysaccharide were identified as independent predictors for ICAE.
Conclusion
These results suggest that there may be a pathophysiological relationship between increased intestinal permeability and ICAE.
Açıklama
Anahtar Kelimeler
Coronary Artery Disease, Isolated Coronary Artery Ectasia, Intestinal Permeability, Lipopolysaccharide, Low-Grade Endotoxemia, Zonulin
Kaynak
Coronary Artery Disease
WoS Q Değeri
Q3
Scopus Q Değeri
Q3
Cilt
34
Sayı
2
Künye
Toprak, K., Kaplangoray, M., Altiparmak, I. H., Taşcanov, M. B., Güngören, F., Fedai, H., ... & Demirbağ, R. (2023). Can increased intestinal permeability and low-grade endotoxemia be the triggering pathogenesis in isolated coronary artery ectasia?. Coronary Artery Disease, 34(2), 102-110.
